A recombinant microorganism displays a fusion protein on its surface to induce an immune response.
Extracellular enzyme secretion converts lysine to cadaverine, reducing intracellular accumulation and lowering purification costs.
Fusing chorionic gonadotropin carboxy-terminal peptides to Factor VII extends circulation time, reducing dosing frequency for hemophilia treatment.
Administering a PTPσ inhibitor restores sympathetic innervation, reducing arrhythmia susceptibility and normalizing cardiac electrophysiology.
Hijacking ERAD machinery with a viral glycoprotein construct removes TCR and HLA expression, preventing GVHD in allogeneic therapy.
A dual-target chimeric antigen receptor recognizes both CD19 and CD22 antigens on tumor cells to enhance killing efficacy.
A high-throughput screening method evaluates diverse chimeric antigen receptor libraries to identify functional candidates.
A recombinant measles virus expresses a ubiquitin-fused hTERT antigen to stimulate broad T-cell immunity.
Engineered anti-MUC1 CAR-T cells resolve off-tumor toxicity by targeting unique tumor-specific MUC1 glycoforms.
Fusion peptide inhibiting PI3Kγ kinase-independent function increases cAMP levels, addressing β2-AR desensitization and PDE4 side effects.
Bispecific CAR T cells targeting PSCA and PSMA resolve diagnostic specificity limits by eliminating recurrent prostate cancer.
Mutant HBV polymerase polypeptide induces strong T-cell immunity, resolving temporary efficacy and side effects from chronic cccDNA persistence.
Modified T cells expressing a secretable anti-SIGLEC-15 scFv resist PD-1-mediated suppression, restoring cytokine production and anti-tumor efficacy.
Truncating the SOCS3 SH2 domain removes destabilizing PEST motifs, enabling soluble expression and competitive inhibition of leptin receptor degradation.
YY1 and EZH2 inhibitors downregulate expression in T cells to reverse exhaustion caused by persistent activation.
Hybridizing oligonucleotides reversibly modify cell surface proteins, enabling dynamic control over cellular processes without permanent structural alteration.
Anti-IL1RAP antibodies selectively eliminate leukemia stem cells while sparing normal hematopoietic tissue through bispecific T-cell engagement.
Modified intracellular signaling domains reduce cytokine release syndrome while maintaining targeted tumor killing activity.
EPRS fragment binds PCBP2 to protect MAVS signaling proteins from degradation, enabling robust innate immune activation against viral threats.
A universal CAR-NK cell recognizes a common hapten to redirect immune targeting toward diverse HIV epitopes.
M200 mutations in APRIL increase BCMA binding affinity while reducing TACI cross-reactivity to spare non-cancerous B and T cells.
Dual CAR T cells targeting ROR1 and CD19 prevent antigen escape while minimizing off-target cytotoxicity.
A fluorescent fusion polypeptide changes localization from the cell membrane to retention vesicles upon second messenger binding.
BATF and IRF4 expression in CAR T cells reduces inhibitory markers like PD-1, TIM3, and LAG3 to sustain anti-tumor efficacy.
Dual targeting drug carriers use segmented peptides to bind tumor and vascular endothelial cells, reducing healthy tissue damage from non-specific delivery.
Synthetic peptide combining PD-1 signal sequence with cell-penetrating peptide suppresses tumor cell proliferation.
PTD-HMGB1A pretreatment inhibits HMGB1 secretion, reducing immunological rejection and increasing engraftment success.
Genetic modification of T cell homing receptors alters trafficking pathways to specific tissues.
Novel bacterial secretion signal sequences direct recombinant proteins to the periplasmic space for proper processing.
Codon optimization and a specific signal peptide enable high-yield phytase secretion in Aspergillus niger, eliminating methanol safety hazards.
pH-dependent binding affinity in acidic tumor microenvironments reduces off-target effects while maintaining cytotoxic activity.
Modified eIF4G1 peptide stabilizes alpha-helix structure to enhance binding affinity with eIF4E, disrupting cap-dependent translation in cancer cells.
Fusing a macromolecule transduction domain to Cas9 resolves low solubility and yield issues while enabling efficient gene editing.
Modifying the alkaline phosphatase signal peptide prevents proteolytic degradation of proMMP-7 in E. coli, enabling high-yield production.
Segmented CaM-KIIN-derived peptides target CaMKII specifically, avoiding side effects on other kinases.
Conjugated TAT-GABARAPL2 peptide inhibits ATG4 proteolytic activity, suppressing cancer cell viability and tumor growth.
A recombinant host cell reduces FLO8 expression and uses a glucose-regulatable promoter for heterologous protein production.
Engineered synthetic mRNA delivers reprogramming factors to induce pluripotent stem cells, eliminating viral integration risks and feeder cell requirements.
Fusion molecules exploit bacterial toxins to bypass endosomal degradation, enabling efficient cytosolic delivery of non-natural peptides.
Replacing chemical demethylation with biological pathways in modified host cells reduces toxic waste while improving benzylisoquinoline alkaloid yields.
A chimeric cytokine receptor merges GM-CSF binding with IL-18 signaling to boost therapeutic immune cell expansion and persistence.
An ICOS domain chimeric antigen receptor boosts Th17 cell persistence.
AAC-11 peptides disrupt cancer cell plasma membranes to induce rapid cell death, overcoming treatment resistance in tumors with disrupted pathways.
Site-specific nucleases target eukaryotic genomic loci to integrate binder genes with high precision.
Modular segmentation of TRAIL homology domains with flexible linkers improves thermal stability, extending serum half-life for cancer treatment.
Engineered Saccharomyces yeast cells produce hyaluronic acid using specific enzymatic pathways for bio-manufacturing.
A peptide sequence inhibits PSD-95 binding to NMDAR 2B receptors.
Humanized LAG3 animal models replicate human immune responses, resolving species differences that compromise drug screening reliability.
Engineering stem cells with suppressed B2M and CIITA genes eliminates immune rejection, enabling cost-effective universal CAR-T treatments.